Search

Objective To evaluate serum levels of adiponectin in pregnant adolescents between 30 and 36 weeks of gestation. Method: A prospective cross-sectional study enrolled 67 normal pregnant women between 30 and 36 weeks of gestation and eutrophic (body mass index [BMI]: 18.5-25 kg/m2), of which 36 were adolescents (< 20 years old) and 31 adults (≥ 20 years old). Serum adiponectin levels were determined by enzyme-linked immunosorbent assay (ELISA). The t-student or Mann-Whitney tests were used for intergroup comparison. Results Pregnant adolescents showed significantly higher serum adiponectin concentrations comparedwith pregnant adults (p=0.04). No differences were observed in adiponectin levels in younger pregnant adolescents (< 16 years old) compared with older pregnant adolescents (≥ 16 years old). Adiponectin values were divided into 3 subgroups:5,000 ng/mL. Birthweight was significantly higher in women>5,000 ng/mL when compared with5.000 ng/mL. O peso do recém-nascido foi significantemente maior nas mulheres com>5.000 ng/mL, quando comparadas as com

To assess maternal serum levels of vitamin D in fetuses appropriate for gestational age (AGA), small for gestational age (SGA), and with fetal growth restriction (FGR) according to estimated fetal weight (EFW). This cross-sectional study included 87 pregnant women between 26 and 36 weeks of gestation: 38 in the AGA group, 24 in the SGA group, and 25 in the FGR group. Maternal serum vitamin D levels were assessed using the chemiluminescence method. The Fisher exact test was used to compare the results between the groups. The mean ± standard deviation (SD) of maternal age (years) and body mass index (kg/m Maternal serum vitamin D levels did not present significant differences among pregnant women with AGA, SGA, or FGR fetuses between 26 and 36 weeks of gestation according to EFW. Avaliar o nível sérico materno de vitamina D em fetos adequados para idade gestacional (AIG), pequenos para idade gestacional (PIG) e com restrição de crescimento (RCF) de acordo com a estimativa de peso fetal (EPF). MéTODOS: Realizou-se um estudo transversal envolvendo 87 gestantes entre 26 e 36 semanas, sendo: 38 do grupo AIG, 24 do grupo PIG e 25 do grupo RCF. A dosagem sérica materna de vitamina D foi realizada pelo método de quimiluminescência. Para as comparações entre os grupos, utilizou-se o teste exato de Fisher. A média ± desvio-padrão (DP) da idade materna (anos) e do índice de massa corporal (kg/m

Gestational diabetes mellitus (GDM) has been associated with impaired maternal immune response. Our aim was to review the available literature linking immune cells profile to GDM, in order to comprehend the role that different subpopulations play in the development of this pathology. We searched in PubMed for studies published in the last decade on circulating levels and placenta expression of immune cells on GDM. We identified 18 studies with several differences regarding the study design, clinical characteristics, number of participants, cell subpopulation and type of sample. Most studies assessed only one subpopulation either in peripheral blood or placenta and did not analyse functional properties of the cells. The most frequently evaluated immune cells were T lymphocytes, especially regulatory T (Tregs), and natural killer (NK) cells in the peripheral blood, and placental macrophages. No studies analysing B cells were identified, and only one study each evaluating γδT cells, dendritic cell (DC) and monocytes was found. Although there are controversies, at least one study reported positive association between GDM and CD4+ (activated), Tregs, Th17 and γδT cells; neutrophil/lymphocyte; NK cell (cytotoxic); macrophages; and monocytes. The number of studies is still small, so caution should be exercised in interpreting the data, and further research is required to validate these findings and establish the role of adaptive and innate immune cells in GDM pathophysiology.

Gestational diabetes mellitus (GDM), the major endocrine pathology in pregnancy, has been associated with the development of an intense inflammatory process and increased insulin resistance. The maternal microbiota is involved in several metabolic functions; however, its role in GDM physiopathology remains unclear. The aim of this study was to assess the composition of the microbiota at different sites and evaluate its relationship with the occurrence of GDM. This cross-sectional study recruited women in the third trimester of gestation with and without GDM. Oral, vaginal, and stool samples were evaluated using next-generation sequencing. We included 68 participants: 26 with and 42 without GDM. The analysis of the oral microbiome did not show significant differences in phyla and genus among the studied groups. In contrast, GDM patients presented a specific vaginal and intestinal microbiome composition, which was less diverse than those found in the control group, showing genera related to dysbiosis. Our findings suggest that changes in the composition of the vaginal and intestinal microbiome might be involved in the development of GDM. The follow-up of these patients in order to evaluate vaginal and intestinal samples after delivery may contribute to understanding the development of metabolic disease in women with previous GDM.

Problem From conception, a delicate regulation of galectins, a family of carbohydrate-binding proteins, is established to ensure maternal immune tolerance in pregnancy. Though galectin-3 (gal-3), the only chimera-type galectin, is abundantly expressed at the feto-maternal interface; the physiological role of this lectin during pregnancy remains to be fully elucidated and requires further investigation. Method of study In this study, we analyzed serum gal-3 levels during the course of healthy gestation. Trophoblast functions were evaluated upon gal-3 exogenous stimulation using trophoblastic cell lines (e.g. , HIPEC65, SGHPL-4, and BeWo cells). Finally, we investigated variations in peripheral gal-3 levels associated with the development of spontaneous abortion and gestational diabetes mellitus (GDM). Results Gal-3 circulating levels increased as normal pregnancy progressed. In vitro experiments showed that exogenous gal-3 positively regulated trophoblast functions inducing invasion, tube formation, and fusion. Compared with normal pregnant women, circulating gal-3 levels were significantly decreased in patients who developed GDM. Conclusion Our results reveal a physiological role for gal-3 during pregnancy, promoting proper trophoblast functions associated with healthy gestation. GDM is associated with a failure to increase circulating gal-3 levels late in gestation. Thus, dysregulation of gal-3 may indicate a contribution of the chimera-type lectin to this adverse pregnancy outcome.

Objective To evaluate the relationship between vitamin D receptor (VDR) gene polymorphism (FokI [rs10735810]) and serum vitamin D concentration in gestational diabetes mellitus (GDM). Methods A prospective case-control study that recruited healthy pregnant women (control group) (n = 78) and women with GDM (GDM group) (n = 79), with no other comorbidities. Peripheral blood samples were collected in the 3rd trimester of gestation, and all of the pregnant women were followed-up until the end of the pregnancy and the postpartum period. Serum vitamin D concentrations were measured by high-performance liquid chromatography (HPLC). For genomic polymorphism analysis, the genomic DNA was extracted by the dodecyltrimethylammonium bromide/ cetyltrimethylammonium bromide (DTAB/CTAB) method, and genotyping was performed by the polymerase chain reaction - restriction fragment length polymorphism (PCR-RFLP) technique, using the restriction enzyme FokI. The Student-t, Mann- Whitney, chi-squared, and Fischer exact tests were used for the analysis of the results. Results There was no significant difference between the pregnant women in the control and GDM groups regarding serumvitamin D levels (17.60 ± 8.89 ng/mL versus 23.60 ± 10.68 ng/mL; p = 0.1). Also, no significant difference was detected between the FokI genotypic frequency when the 2 groups were compared with each other (p = 0.41). Conclusion There was no association between the FokI polymorphism and the development of GDM, nor was there any change in serum vitamin D levels in patients with GDM. Resumo Objetivo Avaliar a relação entre o polimorfismo do gene receptor da vitamina D (VDR) (FokI [rs10735810]) e a concentração sérica de vitamina D no diabetes mellitus gestacional (DMG). Métodos Estudo prospectivo tipo caso-controle que recrutou gestantes saudáveis (grupo controle) (n = 78) e com DMG (grupo DMG) (n = 79), sem outras comorbidades. Foram coletadas amostras de sangue periférico no 3° trimestre da gestação, e todas as gestantes foram acompanhadas até o final da gravidez e no pós-parto. As concentrações séricas de vitamina D foram mensuradas por cromotografia líquida de alta eficiência (CLAE). Para análise do polimorfismo genético, o DNA genômico foi extraído pelo método de brometo de dodeciltrimetilamônio/brometo de cetiltrimetilamônio (DTAB/CTAB), e as genotipagens foram realizadas por técnica de reação de cadeia de polimerase - polimorfismo do comprimento do fragmento de restrição (PCRRFLP, na sigla em inglês), sendo empregada a enzima de restrição FokI. Foram utilizados os testes t-Student, Mann-Whitney, qui-quadrado e exato de Fischer para a análise dos resultados. Resultados Não houve diferença significativa entre as gestantes dos grupos controle e DMG quanto aos níveis séricos de vitamina D (17,60 ± 8,89 ng/mL versus 23,60 ± 10,68 ng/mL; p = 0,1). Também não foi detectada diferença significativa entre a frequência genotípica de FokI, quando comparados os 2 grupos entre si (p = 0,41). Conclusão Não foi identificada associação do polimorfismo FokI com o desenvolvimento de DMG, bem como não foi observada alteração nos níveis séricos de vitamina D em pacientes com DMG.

In indicated preterm births such a Gestational Diabetes Mellitus (GDM), little is known about the role of the amnion membranes. Investigating the role of amnion membrane inflammation in response GDM may suggest novel pathophysiologic mechanisms. We hypothesize that increased GDM inflammatory mediators may weaken the amnion membrane predisposing them to infection. Maternal and fetal serum and amnion membrane biopsies were collected from 20 GDM and 38 normoglycemic subjects (control) who underwent elective cesarean sections. Cytokines and adipokines were evaluated in serum and amnion culture supernatant samples. Amnion membrane biopsies from GDM and control subjects were studied: fresh frozen for RNA analysis for Toll-like receptor expression; cultured with LPS to test membrane permeability, and inflammation LPS + anti-TLR4 for testing mechanism. GDM was associated with higher fetal serum leptin (p = 0.004) and IL-10 (p = 0.04) compared to controls. Amnion membrane explants from GDM had higher levels of IL-6 (p = 0.019), and lower expression of Claudin-4 (p = 0.007) and increased permeability (p = 0.046) compared to controls. GDM membranes treated with LPS showed an increased expression of IL-10 (p = 0.013); IL-6 (p = 0.004) and TNF-α (p = 0.0005) but did not affect membrane permeability. LPS and anti-TLR4 antibody treatment reduced the production of TNF-α in controls (p = 0.03) and GDM (p = 0.007) compared to LPS alone. Fetal inflammatory response seems more balanced in GDM and does not impact membrane permeability function even with an infectious stimulus. Light fetal membrane inflammatory response may explain lack of preterm labor in GDM. Concluding, benign inflammation in the membranes may not be harmful for pregnancy maintenance.

Assessing the biochemical markers levels and the uterine artery Doppler (UtA) parameters in fetuses with growth restriction (FGR). Prospective case–control study included 66 patients with diagnosis of FGR and 64 healthy pregnancies at 24–41 weeks of gestation. For both groups, maternal circulating concentrations of biochemical factors of soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin(sEng), adiponectin, A disintegrin and metalloproteinases (ADAM-12), pregnancy-associated plasma protein-A (PAPP-A), angiopoietin-2 (ANGI-2), vascular endothelial growth factor (VEGF) and transforming growth factor-β (TGF-β) were assayed by ELISA and UtA by Doppler were performed. ANOVA, Mann–Whitney tests and Pearson correlation coefficient were applied to compare the biochemical factors, UtA Doppler and EFW Z-score between the groups. Concentrations of sFlt-1, sEng, PAPP-A were significantly higher in FGR than controls (p

Problem Maternal obesity is frequently associated with gestational diabetes mellitus (GDM), and immunological mechanisms seem to be involved in the physiopathology of these conditions. The aim of this study was to characterize the profile of immune cells in peripheral blood of overweight women with GDM. Method of study This case-control study included 27 glucose-tolerant (controls) and 31 GDM overweight pregnant women. Flow cytometry was used to assess the number of regulatory T cells (Treg) and natural killer (NK) cells in the peripheral blood. In addition, the expression of IL-10, TGF-B, and TNF-A in Treg and expression of IFN-G, TNF-A, granzyme, and perforin in NK cells were analyzed. Results GDM patients had significantly lower frequency of TCD4+ CD25bright and TCD4+ CD25+ FOXP3high cells, higher production of TNF-A by Treg cells and higher percentage of NKCD16+ 56dim cells than the controls. Conclusion The association between obesity and GDM is a condition where it is observed impaired Treg and NK cells profile, findings that seem to be related with the development of IR and inflammation.

The study of adipokines in overweight women with early-onset (diagnosed before 20 weeks) gestational diabetes mellitus (GDM) could help to understand the ethiopathological mechanisms of this disorder. Our aim was to assess adipokine levels in overweight pregnant women with early-onset GDM compared to patients with standard-onset (diagnosed at 24–28 weeks) GDM and to glucose-tolerant women at the same gestational ages. This nested case–control study included 133 overweight pregnant women: 33 with early-onset (diagnosed

Objective To assess correlations between maternal serum levels of pro- and anti-angiogenic factors with uterine perfusion in women with early- compared with late-onset preeclampsia, and in healthy pregnant women. Design Case-control study. Setting Antenatal care clinic located within a hospital (Sao Bernardo do Campo, Brazil). Population We enrolled 54 preeclamptic and 54 healthy control women who were coming for routine ultrasound at 28–36 weeks' gestation. Methods All participants had uterine artery and umbilical Doppler studies and a blood sample to assess maternal serum levels of soluble fms-like tyrosine kinase-1, soluble endoglin, adiponectin and plasminogen activator inhibitor-1. All angiogenic factors were measured using enzyme-linked immunosorbent assay. Main outcome measures Levels of pro- and anti-angiogenic factors in maternal serum, and uterine artery Doppler findings. Results Concentrations of soluble fms-like tyrosine kinase-1 and soluble endoglin were significantly higher in preeclamptic than control women (p

Objective Gestational diabetes Mellitus has been considered an inflammatory disease involving different cells and mediators in its development. The role of innate immune cells in GDM physiopathology remains unclear, therefore this study was conducted to assess monocyte profile in GDM patients. Design This was a case-control study including 20 glucose-tolerant pregnant women (controls) and 18 GDM patients. Methods Flow cytometry was used to assess peripheral blood monocytes subsets (classical, intermediate, non-classical), the expression of TLR4 and CCR2 chemokine receptor (CD192) and cytokines (TNFA, IL6, IL10) secretion by monocytes subsets. In addition, sCD14 serum levels were evaluated by ELISA. Results We observed increased percentage of CD14+ cells, decreased frequency of intermediate monocytes (CD14+CD16+), and lower percentage of circulating monocytes (classical, intermediate and non-classical) that express TLR4 in the diabetic group compared to controls. Soluble CD14+ serum levels were higher in GDM patients compared to controls. There were no differences in the expression of the CCR2 chemokine receptor and cytokines (TNFA, IL6 and IL10) secretion between the studied groups. Conclusions Our results demonstrated that GDM patients present impaired monocyte profile in the peripheral blood, suggesting that these cells are involved in GDM physiopathology.

Background Cervical insufficiency is characterized by premature, progressive dilation and shortening of the cervix during pregnancy. If left unattended, this can lead to the prolapse and rupture of the amniotic membrane, which usually results in midtrimester pregnancy loss or preterm birth. Previous studies have shown that proinflammatory cytokines such as interleukin-1β, interleukin-6, interleukin-8, and tumor necrosis factor alpha are up-regulated in normal parturition but are also associated with preterm birth. Studies evaluating such markers in patients with cervical insufficiency have evaluated only their diagnostic potential. Even fewer studies have studied them within the context of cerclage surgery. Objectives(S) The objective of the study was to evaluate the impact of local and systemic inflammatory markers on the pathogenesis of cervical insufficiency and the effect of cerclage surgery on the local immune microenvironment of women with cervical insufficiency. Study Design We recruited 28 pregnant women (12–20 weeks' gestation) diagnosed with insufficiency and referred for cerclage surgery and 19 gestational age–matched normal pregnant women as controls. Serum and cervicovaginal fluid samples were collected before and after cerclage surgery and during a routine checkup for normal women and analyzed using a targeted 13-plex proinflammatory cytokine assay. Results Before surgery, patients with cervical insufficiency had higher levels of interleukin-1β, interleukin-6, interleukin-12, monocyte chemoattractant protein-1 and tumor necrosis factor alpha in cervicovaginal fluid compared to controls, but after surgery, these differences disappeared. No differences were found in serum of insufficiency versus control women. In patients with insufficiency, the levels of interleukin-1β, interleukin-6, interleukin-8, monocyte chemoattractant protein-1, and interferon gamma in cervicovaginal fluid declined significantly after cerclage compared with before intervention, but these changes were not detected in serum. Conclusion Compared with normal women, patients with cervical insufficiency have elevated levels of proinflammatory cytokines in cervicovaginal fluid but not in serum, suggesting a dysregulation of the local immune environment. Cerclage intervention led to a significant decline in these proinflammatory cytokines, suggesting that cerclage may help reduce local inflammation in cervical insufficiency.

The relevance of gene polymorphisms in the development of unexplained recurrent spontaneous abortion is still unclear. Cytokines, angiogenic mediators, and hormones are involved in all stages of reproduction and pregnancy outcome. Impaired production and/or unbalanced ratios of these mediators have been implicated in the pathogenesis of unexplained recurrent spontaneous abortion. Functional polymorphism influence gene activity and therefore can interfere with the expression of mediators. Several studies have been carried out to evaluate the relationship between cytokines, angiogenic mediators, and hormones gene polymorphisms and unexplained recurrent spontaneous abortion. The results of these studies are mostly contradictory, and few significant associations have been identified. Up to present time, the evidence is insufficient to support the evaluation of cytokines, angiogenic mediators, and hormones gene polymorphism in routine workup in all cases of recurrent pregnancy loss, and these tests are not included in any of the major obstetric guidelines.

The incidence of gestational diabetes (GD) is rising worldwide, in parallel with obesity and type 2 diabetes. Obesity and GD are conditions that have in common a state of chronic, low-grade subclinical inflammation characterized by abnormal production of cytokines and mediators. Genetic polymorphisms may influence the production of inflammatory mediators and predispose to different disorders, including diabetes. The aim of this study was to review the existing literature on the relationship between inflammatory mediator gene polymorphisms and GD. The search in PubMed was restricted to articles published in English, from January 1990 to December 2010. Eight studies were included. These publications evaluated 13 different SNPs and six inflammatory mediators in the blood of women with GD. Gene polymorphisms related to leptin, mannose-binding lectin (MBL) and RAGE (receptor for advanced glycation end products) were individually evaluated in a single study each. Leptin and MBL plasma levels were also evaluated in two studies. The participants included in the studies were ethnically different, but matched with controls. Different criteria were adopted to select the participants. Seven of the eight studies included took into consideration the BMI of patients and controls. Due to the heterogeneity and limited number of studies on GD and inflammatory gene polymorphisms, we could not pool together any of the results or perform any additional analyses of the existing data. Since the existing findings come from isolated studies with mostly small sample sizes, there is a need for new, larger, properly designed studies of good methodological quality.

This review summarizes recent findings on the changes that occur during pregnancy in the composition of the vaginal and gut microbiome and their association with metabolic, hormonal, and immunological factors. Despite many studies on the topic, the vaginal and gut microbial profiles and their influence on the course of pregnancy are still unclear. We present data suggesting that, contrary to traditional understanding, the placenta is not sterile but has a microbial community. We review and discuss new findings on changes in the richness and diversity of the microbiota of pregnant women with term or preterm births, obesity, and gestational diabetes mellitus. Several factors influence the bacterial profile of these women and may explain, at least in part, some of the discrepant findings between studies. The development of and access to new molecular biology methods and techniques has expanded the possibilities of research. This will contribute to a better understanding of the microbiome and its role in normal and pathological pregnancies.

Citation Elito J Jr, Daher S, Fernandes da Silva MO, Marconi NMH, Pendeloski KPT, Moron AF, Camano L. Association study of vascular endothelial growth factor and polymorphisms of its gene with ectopic pregnancy. Am J Reprod Immunol 2010; 63: 120–125 Problem In ectopic pregnancy, increased levels of vascular endothelial growth factor are present. The aims of this study were to determine the association between −634C/G, −460T/C, and +936C/T vascular endothelial growth factor (VEGF) polymorphisms and ectopic pregnancy, and to determine whether serum levels of VEGF were affected by genetic factors. Method of study This is a case–control study wherein 74 women with a history of ectopic pregnancy in a tertiary care center were compared to 134 post-menopausal controls with two pregnancies and no ectopic pregnancy for the genotyping of VEGF polymorphisms. For 35 patients with the diagnosis of ectopic pregnancy, serum concentrations of VEGF were obtained before the treatment. Genotyping of VEGF (−634C/G, −460T/C, and +936C/T) polymorphisms was performed by PCR, followed by endonuclease digestion. ELISA was performed to evaluate the VEGF serum levels. Results The −634C/G, −460T/C, and +936C/T VEGF polymorphisms were not associated with ectopic pregnancy (P = 0.170, P = 0.285, and P = 0.700, respectively). The serum levels of VEGF were not associated with the genotype of −634C/G, −460T/C, and +936C/T VEGF polymorphisms (P = 0.702; P = 0.347, and P = 0.256, respectively). Conclusion There was no association between ectopic pregnancy and −634C/G, −460T/C, and +936C/T VEGF polymorphisms. There was no correlation between VEGF genotype and the expression of VEGF in blood samples.

The clinical spectrum of preeclampsia (PE) ranges from mild hypertension to severe vasospasm associated with convulsions and multiple organ damage. The biological factors that determine the progression of PE to eclampsia (E) are unknown. Endothelial cell activation seems related to an impaired maternal immune response. The production of cytokines, IL-10 and TGF-beta1, is apparently suppressed, and altered IL-2/IL-10 and TNF-alpha/IL-10 ratios have been reported in preeclamptic cases. The relationship between PE and cytokine gene polymorphism has been studied, but there are few studies that include eclamptic patients. This study aimed at investigating whether polymorphisms in genes, TNF-alpha promoter (-308 GA), IL6 promoter (-174 GC), IFN-gamma intron 1 (+874 AT), IL10 promoters (-1082 AG), (-819 CT) and (-592 CA) and TGF-beta1 codon 10 (+869 TC) and codon 25 (+915 GC) are associated with E and/or PE. Genotyping was carried out in 266 Mulatto women from the northeastern region of Brazil who were referred to a single maternity hospital: 92 with PE, 73 with E and 101 normotensive controls. The chi(2) or Fisher's exact tests were used to compare genotype frequencies. Among the six single-nucleotide polymorphisms (SNPs) studied, we found no difference in genotype frequencies between the groups. There was a higher frequency of IFN-gamma (+874 A) in eclamptic patients in comparison with that in controls. (70.3 vs. 57.8%, respectively; P=0.02). There were no other significant differences in allelic frequencies between eclamptic, preeclamptic and control groups We found no independent association between any single SNP and PE or E risk in this population of Mulatto women from the northeastern region of Brazil.

The incidence of melanoma is increasing worldwide. It is one of the leading cancers in pregnancy and the most common malignancy to metastasize to placenta and fetus. There are no publications about experimental models of melanoma and pregnancy. We propose a new experimental murine model to study the effects of melanoma on pregnancy and its metastatic process. We tested several doses of melanoma cells until we arrived at the optimal dose, which produced tumor growth and allowed animal survival to the end of pregnancy. Two control groups were used: control (C) and stress control (SC) and three different routes of inoculation: intravenous (IV), intraperitoneal (IP) and subcutaneous (SC). All the fetuses and placentas were examined macroscopically and microscopically. The results suggest that melanoma is a risk factor for intrauterine growth restriction but does not affect placental weight. When inoculated by the SC route, the tumor grew only in the site of implantation. The IP route produced peritoneal tumoral growth and also ovarian and uterine metastases in 60% of the cases. The IV route produced pulmonary tumors. No placental or fetal metastases were obtained, regardless of the inoculation route. The injection of melanoma cells by any route did not increase the rate of fetal resorptions. Surprisingly, animals in the IV groups had no resorptions and a significantly higher number of fetuses. This finding may indicate that tumoral factors released in the host organism to favor tumor survival may also have a pro-gestational action and consequently improve the reproductive performance of these animals.

Aim: Considering the roles of c-erB-2 and p53 oncoproteins in tumor progression, we aimed to evaluate their expression in hydatidiform moles, and the possible predictive value of this immunoexpression in postmolar follow-up. Methods: Group I comprised 35 patients with progression to gestational trophoblastic tumor, and group II included 32 patients with progression to spontaneous remission. Immunohistochemical tests were performed by streptavidin-peroxidase method. c-erbB-2 immunoexpression was evaluated according to quantitative and semiquantitative criteria; p53 according to percentage of cells with stained nuclei. Data were analyzed by Student t-test, Mann–Whitney test, ROC curve and logistic regression analysis. Results: c-erbB-2 and p-53 expressions were significantly increased in group I. Quantitative and semiquantitative analysis of c-erb-2 showed that its expression may be associated with mole hydatidiform progression to gestational trophoblastic tumor. Taking into account cells with complete membranous delineation we proposed a cut-off value of 10.8%. Similarly, considering the percentage of cells presenting nuclei marked by p53 we suggested a cut-off value of 40.1% for the prediction of malignant transformation of mole hydatidiform. Conclusions: c-erbB-2 and p53 immunoexpression in hydatidiform mole are usually increased with malignant transformation. In addition to β-fraction of human chorionic gonadotropin, they could possibly help the establishment of a therapeutic protocol.

BACKGROUND: In view of evidence suggesting an immunological cause of recurrent spontaneous abortions (RSA) and the large number of maternal natural killer (NK) cells present in the pregnant uterus, we investigated the genetic polymorphism of the killer cell immunoglobulin-like receptors (KIR) in women with RSA. METHODS: KIR gene repertoire and KIR2DL4 (a receptor for HLA-G) genotyping were determined by SSP and SSCP respectively, in women experiencing RSA and controls. RESULTS: The KIR repertoire did not differ between RSA patients and controls in terms of: (i) the number of inhibitory receptors; (ii) the number of activating receptors; (iii) the ratio of inhibitory to activating receptors. KIR2DL4, a receptor for HLA-G, has different transmembrane alleles, which produce functionally different phenotypes. The frequency of KIR2DL4 transmembrane genotypes differed significantly between RSA patients and controls (P = 0.03). However, although homozygosity for a membrane-bound receptor was more frequent in patients (25%) than controls (10%), other genotypes that would produce the same phenotype were not more frequent in patients than controls. CONCLUSIONS: The data provide little evidence that KIR polymorphism plays a role in predisposition to RSA.

Cytokines seem to play a critical role in the pathogenesis of unexplained recurrent pregnancy loss (RPL). Th1 cytokines have been shown to exert deleterious effects on pregnancy, inhibiting foetal growth and development. On the other hand, Th2 cytokines have been associated with successful pregnancy. The purpose of this study was to evaluate cytokine production in women with RPL. The studied group comprised 29 women with RPL, with at least three consecutive spontaneous abortions. The control group included 27 women with a history of successful pregnancies and no miscarriage. We determined IL-6 and TNF-alpha production in peripheral blood cultured with LPS, as well as IFN-gamma and TGF-beta induced by PHA stimulation. Cytokines were measured by enzyme-linked immunoabsorbant assay (ELISA) using commercial kits (RD, Amersham-Pharmacia). Mann-Whitney test was applied to compare differences between groups. The level of significance was defined at P < 0.05. We observed significantly higher levels of IFN-gamma (355.8 pg/ml versus 98.0 pg/ml; P = 0.01) and a trend toward increased TNF-alpha production (2410.2 pg/ml versus1980.2 pg/ml; P = 0.07) in RPL women as compared to controls. In relation to IL-6 and TGF-beta, no significant difference was detected between RPL and control groups. In agreement with experimental observations, our data support the hypothesis of Th1 cytokine involvement in the pathogenesis of RPL.

OBJETIVO: determinar se a prática do sexo oral e vaginal, com ou sem exposição ao ejaculado, diminui a ocorrência de abortamento recorrente. MÉTODO: estudo caso-controle desenvolvido entre maio de 2000 e abril de 2003. Foi aplicado questionário no qual foram assinaladas algumas características de antecedentes clínicos, obstétricos e sexuais da mulher. Foram constituídos dois grupos de estudo: grupo caso, com 116 mulheres com antecedente obstétrico de dois ou mais abortamentos espontâneos, sem a ocorrência prévia de gestação acima de 22 semanas, e grupo controle, com 241 mulheres cujo antecedente obstétrico mostrasse uma ou mais gestações a termo com filho vivo e sem a presença de abortamentos. As variáveis analisadas relacionaram-se ao número de parceiros com os quais a mulher manteve relações sexuais, uso rotineiro de preservativo masculino, prática de sexo oral e exposição da mucosa oral feminina ao material ejaculado. RESULTADOS: relataram somente um parceiro 38,8% das mulheres do grupo caso e 35,7% das do grupo controle. Em ambos os grupos cerca de 75% das mulheres relataram que seus parceiros não usavam rotineiramente preservativo. Aproximadamente 55% das mulheres de ambos os grupos referiram que praticavam sexo oral, sendo que 13,8% das com aborto de repetição e 20,3% das com história de sucesso gestacional o faziam com exposição da mucosa oral ao ejaculado. Não houve diferença entre as pacientes com aborto de repetição e as com sucesso gestacional quanto ao número de parceiros, uso de preservativo, prática de sexo oral e exposição da mucosa oral ao ejaculado pelo parceiro. CONCLUSÃO: nossos resultados não confirmam a hipótese de que o comportamento sexual tenha influência sobre a ocorrência do aborto espontâneo de repetição. PURPOSE: to evaluate whether oral and vaginal sex practice, with or without exposure to semen, decrease the occurrence of recurrent spontaneous abortion. METHOD: this was a case-control study carried out between May 2000 and April 2003. A questionnaire was applied analyzing the clinical, obstetric and sexual history of women, who were divided into two groups: a case group comprised 116 patients with a history of at least two spontaneous abortions, without previous pregnancy longer than 22 weeks, and a control group that included 241 women with history of one or more term pregnancies with live birth and no miscarriage. The analyzed variables included the number of sexual partners, condom use, oral sex practice, and the exposure of female oral mucosa to semen. RESULTS: in the control group 38.8%, and in the patients group 35.7% of the women had only one partner. In both groups about 75% of the women reported that the partners did not use condom. Approximately 55% of the women of both groups referred oral sex practice, and 13.8% of those with recurrent abortion and 20.3% with a history of successful pregnancies had oral mucosa exposed to semen. There was no difference between the patients with recurrent abortion and women with successful pregnancies regarding number of sexual partners, use of condom, practice of oral sex, and exposure of oral mucosa to the partner's semen. CONCLUSION: our results did not confirm the hypothesis that sexual behavior influences the occurrence of spontaneous abortion. Universidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Departamento de Obstetrícia UNIFESP, EPM, Depto. de Obstetrícia SciELO

The link between maternal obesity and inflammatory mediators is still unclear. Our aim was to summarize the main findings of recently published studies on this topic. We performed a search in Medline for studies published in the last years on obesity, human pregnancy, and inflammatory mediators. We report the findings of 30 studies. The characteristics and number of participants, study design, gestational age at sample collection, and type of sample varied widely. Approximately two-thirds of them investigated more than one mediator, and 50% included participants in only one trimester of pregnancy. The most frequently investigated mediators were leptin, tumour necrosis factor-alpha (TNF-α), and interleukin (IL)-6. Almost all studies reported an association between maternal obesity, leptin, and C-reactive protein (CRP) serum levels but not with IL-1β and IL-10. The association of IL-6, TNF-α, monocyte chemo-attractant protein-1 (MCP-1), adiponectin, and resistin with maternal obesity is still controversial. To clarify the physiopathological link between maternal obesity and inflammation, more high-quality studies are needed.

Cow's milk protein (CMP) allergy was investigated in 25 children (age-range 3 months to 11 years) with chronic constipation. A diagnosis of constipation was made on the basis of a history of painful elimination of hard stools for at least 1 month, whether or not associated with a reduced frequency of stools or soiling. The children were evaluated using clinical parameters and the following laboratory tests: total serum immunoglobulin E (IgE); specific IgE (radioallergosorbent test [RAST]) for whole cow's milk, alpha-lactoalbumin, beta-lactoglobulin, and a food group; and skin-prick tests with whole milk, alpha-lactoalbumin, beta-lactoglobulin, and casein. Following the evaluation, the children were submitted to a CMP-free diet for a period of 4 weeks. In seven patients (28%), constipation disappeared during the CMP-free diet and reappeared within 48-72 h following challenge with cow's milk. In two infants a rectal biopsy revealed allergic colitis and they therefore did not undergo the challenge. High serum levels of total IgE were observed in five of the children who showed a clinical improvement (71%), a positive skin-test in two (29%), and detectable specific IgE in two (29%). These results suggest that CMP allergy or intolerance should be considered as a cause of chronic refractory constipation in children, although the underlying mechanism still require further investigation.

Problem Gestational diabetes mellitus (GDM) is an inflammatory condition that involves unbalanced cytokine production. We carried out a systematic review on the relationship between GDM and maternal circulating levels of cytokines in the 2nd/3rd trimesters. Method of Study Three electronic databases (MEDLINE, EMBASE and LILACS), were searched. Duplicate study selection, extraction and quality assessment was performed. Results Twenty-two studies with 1982 participants reporting levels of 9 cytokines (IL-1B, IL-2, IL-6, IL-10, IL-13, IL-18, IFN-G, TGF-B and TNF-A) were included. Most studies differed considerably in selection criteria, sampling and assay methods and in reporting their results. Consequently, only two studies could be pooled: TNF-A concentration was slightly higher in GDM than in control patients, although not significant (WMD = 0.45, 95% CI −0.34–1.23). Conclusions New studies with well-defined, more homogeneous methodological parameters are needed to detect whether there are significant differences in circulating levels of cytokines in patients with GDM.

Gestational diabetes (GD) exposes mothers and infants to the risk of immediate and later adverse outcomes. Increased insulin resistance is a common feature of GD and obesity. Because of its critical role in regulating insulin sensitivity, resistin has been implicated in the physiopathology of GD. The aim of this study was to review the existing literature on the relationship between circulating maternal resistin levels and GD. Three electronic databases (MEDLINE, EMBASE, and LILACS) were searched for pertinent studies published from 2001 to 2012, without language restrictions. Eleven studies, with a total of 639 participants between 23 and 41 weeks of gestation, were included. The number of GD patients per study ranged from 11 to 81, with varying degrees of disease severity and several different GD diagnostic criteria. Mean concentrations of resistin varied widely both in control women (0.05–22.21 ng/ml) and in GD patients (0.05–62.38 ng/ml). We performed a meta-analysis including a total of 10 studies, and also subgroup analyses according to gestational age at sample collection (up to 32 and >33 weeks). The pooled absolute mean difference (WMD) in resistin levels was slightly lower in GD patients than in controls, but this did not reach statistical significance (WMD = −0.02, 95% CI −0.07 to 0.04). According to the data from the 11 studies analyzed, there was no association between circulating resistin levels and GD. However, this result should be interpreted with caution owing to the large heterogeneity amongst the existing published studies.

Objective. To assess a possible relation between proinflammatory mediators (IL-1R1, IL-12, IL-18, TLR-2, and TLR-4) gene polymorphisms and preeclampsia (PE). Methods. Genotyping was performed on 109 preeclamptic patients and 174 healthy fertile women with at least two previous successful pregnancies (controls). χ2 or Fisher's exact test were used to compare genotype frequencies. The control group included 174 pregnant women matched by race to the study group. Results. Genotypic and allelic distributions for all six polymorphisms were similar between the study and control groups. IL-1R1 (PstI, rs2234650): p = 0.82 ; IL-12 (+1188, rs3212227): p = 0.93; IL-18 (−137, rs187238): p = 0.74 ; IL-18 (−607, rs1946519): p = 0.22; TLR-2 (+2258, rs5743708): p = 0.97; and TLR-4 (+896, rs4986790): p = 0.23. Conclusion. The analyzed gene polymorphisms are not associated with PE.

We evaluated the diagnostic accuracy of Rh blood group, D antigen (RHD) fetal genotyping, using real-time polymerase chain reaction in maternal blood samples, in a racially mixed population. We performed a prospective study conducted between January 2006 and December 2007, analyzing fetal RHD genotype in the plasma of 102 D− pregnant women by real-time polymerase chain reaction, targeting exons 7 and 10 of the RHD gene. Genotype results were compared with cord blood phenotype obtained after delivery or before the first intrauterine transfusion when necessary. Most of the participants (75.5%) were under 28 weeks of pregnancy, and 87.5% had at least one relative of black ancestry. By combining amplification of two exons, the accuracy of genotyping was 98%, sensitivity was 100%, and specificity was 92%. The positive likelihood ratio was 12.5, and the negative likelihood ratio was 0. The two false-positive cases were confirmed to be pseudogene RHD by real-time polymerase chain reaction. There were no differences between the patients with positive or negative Coombs test ( P = 0.479). Determination of fetal RHD status in maternal peripheral blood was highly sensitive in this racially mixed population and was not influenced by the presence of antierythrocyte antibodies.

To examine the association between high prepregnancy maternal body mass index (BMI) and the risk of preterm birth (PTB).A systematic review of the literature. We included cohorts and case-control studies published since 1968 that examined the association between BMI and PTB of all types, spontaneous (s), elective and with ruptured membranes (PPROM) in three gestational age categories: general (37 weeks), moderate (32-36 weeks) and very (32 weeks) PTB.20,401 citations were screened and 39 studies (1,788,633 women) were included. Preobese (BMI, 25-29.9) and obese I (BMI, 30-34.9) women have a reduced risk for sPTB: AOR = 0.85 (95% CI: 0.80-0.92) and 0.83 (95% CI: 0.75-0.92), respectively. Their risk for moderate PTB was 1.20 (95% CI: 1.04-1.38) and 1.60 (95% CI: 1.32-1.94), respectively. Obese II women (BMI, 35-40) have an increased risk for PTB in general (AOR = 1.33, 95% CI: 1.12-1.57) moderate (AOR = 2.43, 95% CI: 1.46-4.05) and very PTB (AOR = 1.96, 95% CI: 1.66-2.31). Obese III women (BMI40) have an even higher risk for very PTB (AOR = 2.27, 95%CI: 1.76-2.94). High BMI does not modify the risk for PPROM and increases the risk for elective PTB.High maternal BMI may have different effects on different types of PTB.

Objective: The aim of this study was to evaluate the production of tumor necrosis factor (TNF) by peripheral blood cells during pregnancy, at the onset of labor and of spontaneous abortion (SA), as well as in non-pregnant women with and without a history of recurrent spontaneous abortions (RSA). Study design: The peripheral blood cells TNF production was evaluated in 28 women in the 1st trimester of pregnancy, 21 in the 2nd, and 30 in the 3rd, 47 at term labor; 43, at the onset of SA; 19 healthy and 19 RSA non-pregnant women. The statistical method used was the Mann–Whitney test. Results: We observed (1) lack of TNF detection in the 1st gestational trimester; (2) increase of TNF production with gestational age, with the highest values being observed at labor (P

The objective was to search for an association between spontaneous preterm birth (sPTB) and single and/or combined polymorphisms in genes TNFA -308 G>A, IL10 -1082 G>A, IL10 -819 C>T, IL10 -592 C>A, IL6 -174 G>C, and IFNG +874 A>T. Genotyping was performed on 410 Brazilian ethnically matched women managed at two hospitals (two independent case-control sets). One set consisted of 122 cases and 101 controls, and the other set comprised 82 cases and 105 controls. We compared genotype and genotype-combination frequencies between cases and controls using Fisher's exact or the chi(2) tests and confirmed results using logistic regression. Among the six SNPs studied, we found no independent association between any single SNP and sPTB risk. The multi-locus analysis revealed a significant association between sPTB and the TNFA(GG)/IL6(GG)/IFNG(AA) genotype combination (p=0.002), confirmed by logistic regression. Our data suggest that the combination of TNF-alpha, IFN-gamma, and IL-6 maternal gene polymorphisms might contribute to susceptibility to sPTB. This finding could be investigated as a possible genetic marker for the risk of spontaneous preterm birth.

s / Placenta 36 (2015) 469e521 519 PB.43. VITAMIN D AND GESTATIONAL DIABETES MELLITUS: PHENOTYPE AND GENOTYPE ANALYSIS K.P.T. Pendeloski, T.F. Lobo, C.M.Y. Ohki, T.W. Siqueira, J.F. Fantasia, M.R. Torloni, R. Mattar, S. Daher. Department of Obstetrics, Universidade Federal de S~ ao Paulo, Sao Paulo, Brazil Objectives: Patients with Gestational Diabetes Mellitus (GDM) have an inflammatory process and insulin resistance which are more intense than women having a physiological pregnancy. Vitamin D plays a role in the control of both inflammation and insulin resistance. Polymorphism in the vitamin D VDR Fok-I gene may affect the expression of this molecule. We evaluated the levels of soluble vitamin D and vitamin D VDR (Fok-I rs10735810) gene polymorphism in GDM patients and healthy controls. Methods: This case-control study included 108 participants in the third trimester of pregnancy: 58 healthy women (control group) and 50 with GDM. Vitamin D serum levels were determined by HPLC. Polymorphism genotyping was obtained by PCR-RFLP. Data were analyzed by Student t and Chi-square tests and significance was set at p < 0.05. Results: There were no significant differences in vitamin D serum levels between the groups (Control x GDM: 19.95 ± 9.35 ng/mL 23.93 ± 12.21 ng/mL, respectively, p 1⁄4 0.09). Genotypic frequencies of VDR Fok-I were 62% FF, 34% Ff and 4% ff in controls, and 50% FF, 36% Ff and 14% ff in the GDM group (p 1⁄4 0.17). There was no association between GDM and the polymorphism analyzed, or between vitamin D genotype/phenotype. Conclusion: GDM was not associated with differences in vitamin D serum levels or with Fok-I VDR polymorphism. Financial support: CNPq (307337/2012-0). PB.44. DOES IN UTERO EXPOSURE TO HUMAN CHORIONIC GONADOTROPIN (HCG) HAVE A PROTECTIVE EFFECT ON HORMONAL IMBALANCES IN TRANSGENIC MICE? Laura D. Ratner , Guillermina Stevens , Carla Marcial , Paula Farre , Matti Poutanen , Ricardo Calandra , Ilpo Huhtaniemi , Susana B. Rulli . 1 Institute of Biology and Experimental Medicine (IBYME-CONICET), Buenos Aires, Argentina; Department of Physiology, University of Turku, Finland; 3 Imperial College London, London, United Kingdom We have previously developed a transgenic mouse model for the human chorionic gonadotropin b-subunit (hCGb+), which exhibits constitutively elevated levels of hCG and increased production of testosterone, progesterone and prolactin from early age. The adult females are infertile, obese, and insulin-resistant and develop pituitary and mammary tumors. After normalization of the prolactin levels by treatment with the dopamine agonist cabergoline, these females become fertile. Objective: To analyze the influence of hCG exposure in utero on the reproductive and metabolic function of the female offspring at adulthood. Methods: hCGb+ females pre-treated with cabergoline (500 mg/dose for one week) at 5 weeks of age were crossbred with wild-type FVB/n males (WT). Female offspring were analyzed for reproductive and metabolic functions at adulthood. Results: the offspring were exposed to the effects of elevated levels of maternal hCG during gestation (WT: 1.8 ± 0.1, hCGb+: 23.4 ± 8.5 mIU/ml, p < 0.01), but with normal values of steroids and prolactin. Eighty percent of the transgenic female offspring exhibited normalized pituitary and body weights as well as normal estrous cycles and gonadal function. These mice were fertile, and gave birth to several litters with similar results. The metabolic disturbances, in terms of glucose and insulin tolerance test (p < 0.01), and basal triglyceride levels were also normalized (p < 0.01). Conclusions: We found that hCG hypersecretion during pregnancy had a significant impact on the transgenic offspring’s phenotype. These results suggest that the presence of hCG during gestation may have a protective effect on the transgenic offspring, by preventing them from hormone imbalances, which led to infertility and metabolic disturbances at adulthood. This is the first mouse model in which gestation occurs in the presence of hCG, and paves the way for future investigations related to extragonadal functions of hGC. Further studies are necessary to understand the mechanism involved in this phenomenon. PB.45. IN VIVO ANALYSIS OF OXIDATIVE STRESS RELATIONSHIP IN EMBRYOFETAL PANCREAS DEVELOPMENT OF THE OFFSPRING OF DIABETIC RATS I.L. Iessi , Y.K. Sinzato , F.Q. Gallego , B. Dallaqua , R.L. Amorim , C.E.F. Alves , I.M.P. Calderon , M.V.C. Rudge , D.C. Damasceno . 1 Laboratory of Experimental Research on Gynecology and Obstetrics, Graduate Program on Gynecology, Obstetrics and Mastology, Botucatu Medical School, Brazil; Department of Pathology, Botucatu Veterinary and Zootechnology School, Univ. Estadual Paulista e UNESP, Botucatu, S~ ao Paulo, Brazil Background: Rat offspring exposed to a hyperglycemic intrauterine environment present alterations in pancreatic hormone levels at birth. Our hypothesis is that the association of maternal hyperglycemia and exacerbated oxidative stress status are involved in the embryofetal pancreatic development impairment. Aim: To evaluate the oxidative stress status in embryofetal pancreatic development in hyperglycemic conditions. Methods: The rats were randomly assigned into: Non diabetic (Control 1⁄4 C, glycemia < 120 mg/dL), Mild diabetes (MD e Streptozotocin, 100 mg/kg b.w., sc.) and Severe diabetes (SD e STZ, 40 mg/kg b.w., i.v.). After mating, on days 11.5, 18.5 and 21 of pregnancy, the dams were killed to obtain their embryo/fetal pancreas for antioxidant enzymes expression and for morphological and immunohistochemistry analyses. p < 0.05 was considered as a significant statistical limit. Results: The expression of antioxidant enzymes showed no difference in the embryonic period and the islet number, islet area and the minor diameter also showed no alterations at fetal period in all groups. However, the major diameter was increased in islets of SD fetuses on day 21 of pregnancy in relation to the others. Insulin immunolocalization in the SD and MD groups was decreased as compared to the C group on day 18.5 and the SD group also presented reduction at term in relation to the others. Glucagon immunolocalization was decreased in SD fetuses on day 18.5 of pregnancy in relation to the C group. There was a reduction of in caspase-3 in the SD group on day 18.5 of pregnancy and an increase in the MD group at term compared to the C group. There was no difference in Ki67 compared to the others. Conclusion: The hyperglycemic intrauterine environment caused no alterations in protein expression. However it caused damages in the pancreatic islet morphometry and hormonal immunolocalization in the fetal development, which might contribute to later alterations in adult life. Acknowledgement: FAPESP/Brazil (Process numbers: 2011/18519-7, 2012/ 23642-2). PB.46. INFLUENCE OF TOXOPLASMA GONDII INFECTION IN THE COMMUNICATION BETWEEN HUMAN EXTRAVILLOUS TROPHOBLAST CELLS AND MACROPHAGES P.M. Guirelli , F.C. Oliveira , M.B. Angeloni , B.F. Barbosa , A.O. Gomes , A.S. Castro , P.S. Franco , R.J. Silva , J.R. Mineo , F. Ietta , E.A. Ferro . 1 Laboratory of Histology and Embryology, Institute of Biomedical Sciences, Federal University of Uberlândia, Av. Par a, 1720, 38405-320 Uberlândia, MG, Brazil; 2 Laboratory of Immunoparasitology, Institute of Biomedical Sciences, Federal University of Uberlândia, Av. Par a, 1720, 38405-320 Uberlândia, MG, Brazil; Department of Life Science, University of Siena, Aldo Moro Road 2, Siena, Italy The interaction between human extravillous trophoblast cells and macrophages plays an important role in implantation and placentation during a successful pregnancy. However, any dysfunction in this communication is associated with pregnancy complications. Objectives: The aim of this study was to investigate the influence of Toxoplasma gondii in the occurrence of apoptosis triggered by macrophages in HTR-8/SVneo cells.

The purpose of the present study was to analyze the frequency of HLA-DR and DQ antigens in Brazilian asthmatic children with skin-test and RAST positivity to Dermatophagoides pteronyssinus. The comparison of HLA-DR and DQ antigenic frequencies between patients (n = 30) and controls disclosed a significantly higher HLA-DQ2 frequency in the patients (60% versus 34%, p = 0.013; R. R. = 2.8).

Preeclampsia is a common complication of pregnancy and a major cause of maternal morbidity. It is associated with placental disorder endothelial cell dysfunction and systemic vasospasm. The events leading these alterations remains unclear but it seems that abnormal activation of the immune system play a relevant role in the etiology of preeclampsia. Some reports suggest a trend toward an increasing prevalence of human immunodeficiency virus (HIV) infection in pregnancy. Different studies have evaluated maternal immune response to HIV infection in pregnancy and investigated whether its represents a risk factor for adverse perinatal outcome however controversial results have been obtained. Our purpose was to investigate the rate of preeclampsia in HIV seropositive pregnant women that were referred to Obstetric Outpatient Clinic of UNIFESP-EPM between 2000 and 2002. (excerpt)

PURPOSE: to evaluate whether there is an association between recurrent spontaneous abortion and atopy. METHODS: this was a case-control study with 230 women: 71 with a history of recurrent spontaneous abortion (group A) and 159 with a history of successful pregnancy (group B). The evaluation included a questionnaire in order to investigate the personal history of atopy, considering symptoms of atopic dermatitis, urticaria, rhinitis, asthma, conjunctivitis and gastric or intestinal symptoms. The presence of specific IgE in response to a pool of inhalants, Phadiatop, detected by an enzymatic fluorescence reaction in blood was also investigated. The data were analyzed by Fisher's exact test and a p value < 0.05 was set as level of significance. RESULTS: a positive history of atopy was observed in 57.7% of group A patients and in 55.3% of group B patients. The incidence of positive IgE against Phadiatop was 38% and 33.9% in groups A and B, respectively. Association of allergy disease with positive Phadiatop (presence of specific IgE) was detected in 28.2% of group A and in 22% of group B patients. There was no significant difference between the groups. CONCLUSIONS: we did not observe any association between recurrent spontaneous abortion and atopy.

PP006. The comparison of serum VEGF and sFlt-1 on preeclampsia and eclampsia pregnant woman before and after delivery at Ulin Hospital, Banjarmasin, Indonesia A. Akbar , B. Abimanyu, E.G. Dachlan , A. Abadi 1 (Obstetrics Gynaecologic (Fetomaternal DIvision), Soetomo Hospital University of Airlangga, Surabaya, Indonesia, 2 Obstetrics Gynaecologic (Fetomaternal DIvision), Ulin Hospital, University of Lambung Mangkurat, Banjarmasin, Indonesia)

s / Journal of Reproductive Immunology 101–102 (2014) 40–60 43 whom markers other than interleukins were determined (n=88); first-trimester pregnant women in whom only interleukins were determined (n=80). These subgroups were subsequently divided according to the development of pregnancy in the third trimester. Each subgroup consists of an equal number of pathological and physiological pregnancies. Measured markers: Serum anti-cardiolipin autoantibodies IgG (ACLA-G) and IgM (ACLA-M), interleukins: IL-6, IL-12, IL-15, IL-16, IL-17, IL-18, and IL-23 (by a standard ELISA). Results: In group C the percentage of IL-6 (p=0.002), IL-18 (p=0.016), IL-23 (p=0.002), and ACLA-G (p

The 29th Annual Meeting of the American Society for Reproductive Immunology was held on 5–9 June 2009, in Orlando (FL, USA). Peter Hansen and Mary Brown co-chaired the conference. The co-chairs and a scientific committee put together an outstanding program that included the most contemporary topics in reproductive immunology, with special focus on intrauterine infections and reproductive anomalies. A highlight of the meeting was the pre-meeting postgraduate course, which was attended by a large group of young investigators and trainees. The participants in the postgraduate course and the main meeting represented an international milieu of investigators, students and health professionals.